The DOI matches its Crossref record; 38 of the 38 references it cites were found in a registry or an index.
A novel transformation suppressor, Pdcd4, inhibits AP-1 transactivation but not NF-κB or ODC transactivation
Abstract
Pdcd4 is a novel transformation suppressor that is highly expressed in promotion-resistant (P-) mouse epidermal JB6 cells but not in susceptible (P+) cells. Overexpression of pdcd4 cDNA in stably transfected P+ cells rendered cells resistant to tumor promoter-induced transformation, indicating that elevated expression of Pdcd4 protein is sufficient to suppress neoplastic transformation. To determine whether Pdcd4 suppresses neoplastic transformation through inhibiting known transformation required events, we examined the possibility that pdcd4 inhibited the activation of AP-1 or NF-kappaB dependent transcription or of ornithine decarboxylase (ODC) activity. Activation of AP-1-dependent transcriptional activity was inhibited by pdcd4 expression in a concentration dependent manner. In contrast, Pdcd4 slightly increased NF-kappaB-dependent transcription and did not alter ODC enzymatic activity. Previous studies suggested that activation of AP-1 was required for P+ cell transformation as well as for tumor promotion in vivo. These results indicate that Pdcd4 functions as a transformation suppressor, possibly through inhibiting AP-1 activation in combination with other factors such as enhancing NF-kappaB activation. Pdcd4 may thus constitute a useful molecular target for cancer prevention.
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“PDCD4 does not inhibit NF-κB in mouse JB6 cells where it inhibits AP-1 transactivation and transformation (26).”
From Tumor suppressor PDCD4 inhibits NF-κB-dependent transcription in human glioblastoma cells by direct interaction with p65 (2014) · cites this paper as [26]
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MicroRNA-21 promotes cell transformation by targeting the programmed cell death 4 gene
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“, 2009), a known negative regulator of AP-1 transactivation (Goke et al., 2004; Jansen et al., 2005; Yang et al., 2003; Yang et al., 2001).”
Metadata
- Authors
- Yang, H.-S., Jansen, A. P., Nair, R., Shibahara, K., Verma, A. K., Cmarik, J. L., & Colburn, N. H.
- Affiliations
- Frederick National Laboratory for Cancer Research (US)
- University of Wisconsin–Madison (US)
- Kyoto University (JP)
- Venue
- Oncogene
- Published
- 2001-02-08
- Volume
- 20
- Issue
- 6
- Pages
- 669-676
- ISSN
- 0950-9232 (ISSN-L)
- 1476-5594
- OpenAlex
- W2093224647
- Cited by
- 185
- References
- 38
- Citations by year
- 2026: 1 · 2025: 2 · 2024: 3 · 2023: 1 · 2022: 1 · 2021: 7 · 2020: 2 · 2019: 5 · 2018: 7 · 2017: 8 · 2016: 8 · 2015: 7 · 2014: 17 · 2013: 17 · 2012: 12
- FWCI
- 2.77
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Oncogene (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mechanisms of cancer metastasis
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Signaling Pathways in Disease
- Keywords
- PDCD4, AP-1 transactivation, NF-κB, ornithine decarboxylase, JB6 epidermal cells, transcriptional regulation, cancer prevention, tumor suppressor
- MeSH terms
- Animals, Cell Transformation, Neoplastic, Ornithine Decarboxylase, Proteins, Tetradecanoylphorbol Acetate, Transcriptional Activation, Genes, Tumor Suppressor, NF-kappa B, RNA-Binding Proteins, Transcription Factor AP-1, Apoptosis Regulatory Proteins, Mice
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